EGFR-IN-213

EGFR-IN-213 (compound 8c) (1 h) potently and selectively inhibits EGFR^{L858R/T790M/C797S} kinase with an IC₅₀ of 0.48 nM^[1].
EGFR-IN-213 (72 h) potently inhibits the proliferation of BaF3-EGFR^{L858R/T790M/C797S} cells (IC₅₀ = 0.249 μM) and H1975 cells (IC₅₀ = 0.082 μM), while showing reduced activity against non-target cancer cell lines and negligible toxicity to HEK-293T cells^[1].
EGFR-IN-213 (0.3-1 μM; 24 h) concentration-dependently arrests BaF3-EGFR^{L858R/T790M/C797S} cells in the G1 phase, with stronger activity than Brigatinib (HY-12857) at 0.3 μM and 1 μM^[1].
EGFR-IN-213 (1-9 μM; 48 h) concentration-dependently induces apoptosis in BaF3-EGFR^{L858R/T790M/C797S} cells, with stronger activity than Brigatinib at 1 μM, 3 μM, and 9 μM^[1].
EGFR-IN-213 (0.3-3 μM; 48 h) concentration-dependently induces apoptotic morphological changes in H1975 cells^[1].
EGFR-IN-213 (1-3 μM (BaF3-EGFR^{L858R/T790M/C797S} cells); 0.3-1 μM (H1975 cells); 24 h) concentration-dependently inhibits EGFR phosphorylation in BaF3-EGFR^{L858R/T790M/C797S} cells, and suppresses EGFR, PI3K, and AKT phosphorylation in H1975 cells, with greater potency and selectivity than Brigatinib^[1].
EGFR-IN-213 (1-3 μM; 24 h) concentration-dependently inhibits colony formation by H1975 cells^[1].
EGFR-IN-213 (0.1-1 μM (Transwell migration); 1 μM (wound healing); 24 h (Transwell migration); 48 h (wound healing)) dose-dependently inhibits the migratory capacity of H1975 cells in both Transwell and wound healing assays^[1].
EGFR-IN-213 (0.3-3 μM; 48 h) concentration-dependently inhibits tube formation by HUVECs, demonstrating anti-angiogenic activity^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.